Hippocampal synaptic plasticity and glutamate receptor regulation: influences of diabetes mellitus

Trudeau, François; Gagnon, Sylvain; Massicotte, Guy

doi:10.1016/j.ejphar.2004.02.055

Cited by 151 publications

(86 citation statements)

References 95 publications

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“…10 Furthermore, high-calorie diet impairs learning ability, decreases hippocampal dendritic spine density and impairs LTP at Schaffer collateral-CA1 synapses. 8 As GLP-1 crosses the blood-brain barrier 7 and directly modulates neurotransmitter release and LTP, 6 we assessed effects of peripheral exendin-4 therapy on cognitive function in a mouse model of diet-induced obesity, which exhibits compromised cognitive performance.…”

Section: Discussionmentioning

confidence: 99%

Actions of exendin-4 therapy on cognitive function and hippocampal synaptic plasticity in mice fed a high-fat diet

et al. 2010

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High-calorie diet has been shown to impair learning ability and hippocampal synaptic plasticity in rodents. This study examined effects of daily treatment with the glucagon-like peptide-1 mimetic, exendin-4, on cognitive function and hippocampal synaptic plasticity in a model of diet-induced obesity, which exhibits compromised cognitive performance. Mice fed a high-fat diet were treated with exendin-4 (25 nmol kg À1 bodyweight; twice daily) or saline vehicle (0.9% (w/v) NaCl) over 21 days. In addition to improving metabolic control, exendin-4-treated mice exhibited a marked increase in recognition index highlighting improved learning and memory. High-fat diet resulted in the elimination of in vivo electrophysiological long-term potentiation, which was rescued following exendin-4 treatment. This study shows that exendin-4 therapy improves cognitive function and ameliorates impaired hippocampal synaptic plasticity in dietary-induced obesity.

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Section: Discussionmentioning

confidence: 99%

Actions of exendin-4 therapy on cognitive function and hippocampal synaptic plasticity in mice fed a high-fat diet

et al. 2010

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“…*** Development Department, Islamic Azad University, Damghan Branch, Damghan, Iran. Biessels et al, 1996;Trudeau et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Alteration of Dentate Gyrus Astrocytes in Diabetic Rats: Protective Role of Urtica dioica

et al. 2011

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GOLALIPOUR, M. J.; GHAFARI, S.; LATIFIMOGHADAM, M. H. & KABOLI, S.Alteration of dentate gyrus astrocytes in diabetic rats: Protective role of Urtica dioica. Int. J. Morphol., 29(4):1307-1312, 2011. SUMMARY:Diabetes mellitus can cause astrocytes alterations in the central nervous system. Urtica dioica (Nettle) is among several species listed for their use against diabetes in folk medicine. Therefore, this study was done to evaluate the protective effect of Urtica dioica on astrocytes density of the dentate gyrus in STZ induced diabetic rats. In this experimental study, 21 male albino Wistar rats were randomly allocated equally into normal, diabetic and protective (nettle treated diabetic) groups. Hyperglycemia was induced by streptozotocin (80 mg/kg) in the animals of diabetic and treatment groups. Before induction of diabetes in animals, animals in protective group received hydroalcoholic extract of Urtica dioica (100 mg/kg/BW /day) for five days intraperitoneally. Four weeks after induction of diabetes, animals were sacrificed and coronal sections were taken from the dorsal hippocampal formation of the right cerebral hemispheres and stained with PTAH stain. The area densities of the astrocytes were measured and compared in the three groups (p < 0.05). The number of astrocytes in DG area of controls was 17.72±6.7. The density of astrocytes increased in diabetic (24.26±9.5) in comparison with controls. The density in the nettle treated rats (23.17±5.8) was lower than diabetic rats. This study showed that the administration of U. dioica extract before induction of diabetes can not significantly help compensate for astrocytes in the dentate gyrus of treated rats.

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“…This socalled retrograde transmission participates in both short and long forms of synaptic plasticity thought to be key elements of cognitive behaviour. LTP is impaired in STZ-induced diabetic animals (for review see Trudeau et al, 2004), which also display an impairment of Ca 2+ -dependent regulation of postsynaptic AMPA receptors (Chabot et al, 1997). Since endocannabinoids can facilitate the induction of LTP in the hippocampus via presynaptic blockade of GABAergic neurotransmission (Carlson et al, 2002) the upregulation of presynaptic CB 1 Rs may contribute to restoring normal LTP functions.…”

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confidence: 99%

“…It affects a plethora of tissues and organs, including the brain. "Diabetic encephalopathy" encompasses characteristic biochemical, electrophysiological, morphological and cognitive deficits in diabetic patients (for review see Trudeau et al, 2004). T1D rats display a similar cognitive impairment and display compromised long-term potentiation (LTP) and marked changes in the density of pre-and postsynaptic synaptic markers, decreased cell proliferation, and apoptosis have all been observed in certain cortical regions (Chabot et al, 1997;Grillo et al, 2005;Jackson-Guilford et al, 2000;Li et al, 2002).…”

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confidence: 99%

Increase of cannabinoid CB1 receptor density in the hippocampus of streptozotocin-induced diabetic rats

Duarte¹,

Nogueira²,

Oliveira³

et al. 2007

Experimental Neurology

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In the hippocampus, impaired neurophysiology, compromised neurogenesis, and eventually apoptosis accompany cognitive deficits in insulinopenic (type-1) diabetes (T1D). The underlying pathological mechanisms remain to be defined. The hippocampus has a high density of the cannabinoid type 1 receptor (CB 1 R), which has been shown to control several brain functions affected by diabetes, such as synaptic plasticity, glucose utilisation, memory consolidation and cognition, and maturation and survival of hippocampal neurons. However, the role of this receptor has not been investigated yet in diabetic encephalopathy. We report now that in the streptozotocin animal model of T1D, the hippocampal densities of CB 1 R protein and of specific CB 1 R binding sites are significantly increased both in the nerve terminals and in total membranes (changes between 13% and 38%), whereas CB 1 R mRNA expression is decreased by 25%, suggesting that CB 1 Rs might play a role in diabetic encephalopathy.

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Hippocampal synaptic plasticity and glutamate receptor regulation: influences of diabetes mellitus

Cited by 151 publications

References 95 publications

Actions of exendin-4 therapy on cognitive function and hippocampal synaptic plasticity in mice fed a high-fat diet

Actions of exendin-4 therapy on cognitive function and hippocampal synaptic plasticity in mice fed a high-fat diet

Alteration of Dentate Gyrus Astrocytes in Diabetic Rats: Protective Role of Urtica dioica

Increase of cannabinoid CB1 receptor density in the hippocampus of streptozotocin-induced diabetic rats

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